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The mucoid switch in Pseudomonas aeruginosa represses quorum sensing systems and leads to complex changes to

Ben Ryall1, Marta Carrara1, James E A Zlosnik1

  • 1Department of Life Sciences, Faculty of Natural Sciences, Imperial College London, Sir Alexander Fleming Building, London, United Kingdom.

Plos One
|May 24, 2014
PubMed

Insights

Pseudomonas aeruginosa mucA22 mutants in cystic fibrosis lungs show altered virulence factor production and quorum sensing. This adaptation may drive the mucoid switch during chronic Pseudomonas aeruginosa infections.

Area of Science:

  • Microbiology
  • Bacterial Pathogenesis
  • Cystic Fibrosis Research

Background:

  • Pseudomonas aeruginosa is an opportunistic pathogen causing chronic lung infections in Cystic Fibrosis (CF) patients.
  • MucA mutations leading to a mucoid phenotype (alginate overproduction) are common in CF, correlating with lung function decline.
  • Alginate production is thought to benefit P. aeruginosa in the CF lung environment.

Purpose of the Study:

  • To investigate the stationary phase physiology and virulence factor production of P. aeruginosa mucA22 mutants.
  • To explore the impact of mucA22 mutations on quorum sensing systems and their role in chronic CF infections.
  • To understand the evolutionary implications of mucA22-mediated adaptations in the CF lung.

Main Methods:

  • Phenotypic characterization of mucA22 mutants in stationary phase.
  • Gene expression analysis of virulence factors (cyanide, pyocyanin) and quorum sensing systems (AHL, PQS).
  • Complementation studies using in trans expression of the Vfr transcription factor.

Main Results:

  • MucA22 mutants exhibited altered virulence factor production in prolonged stationary phase compared to wildtype strains.
  • Significant downregulation of AHL- and AQ (PQS)-dependent quorum sensing systems was observed in mucA22 mutants.
  • In trans expression of Vfr restored quorum sensing and virulence factor production in early stationary phase.
  • MucA22 mutation offers an alternative mechanism to lasR mutations for downregulating quorum sensing in chronic infections.

Conclusions:

  • MucA22 mutation in P. aeruginosa leads to complex changes in virulence factor production and quorum sensing during stationary phase.
  • These adaptations may contribute to the persistence and evolution of P. aeruginosa in the CF lung.
  • The mucA22 mutation provides a selection pressure for the mucoid switch, impacting chronic infection dynamics.

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